Clinical review

Allergy and the skin. IIContact and atopic eczema

P S Friedmann. 

	Allergic contact eczema

Eczema is characterised by erythema, pruritus, vesiculation, and, in more chronic forms, scaly desquamation. Contact eczema may be due to chemically induced irritation or allergic sensitisation. Allergic contact eczema is a cell mediated (delayed type) hypersensitivity reaction to environmental chemical "sensitisers." Hence, it occurs at body sites that make physical contact with the eliciting sensitiser. The term dermatitis is often used for eczema caused by exogenous agents.

Prevalence and aetiology
In the working population of Western countries, contact eczema (both irritant and allergic) accounts for 85-90% of all occupational skin disease. Hand eczema has been estimated to affect 2-6.5% of all populations in Western countries.

View larger version (93K): [in this window] [in a new window]   Allergic contact eczema due to nickel in studs and buttons on jeans

Mechanisms
When skin sensitisers penetrate the epidermis, they are taken up by Langerhans' cellsbone marrow-derived members of the macrophage family that function as "professional antigen presenting cells." The Langerhans' cells leave the epidermis and migrate to the regional lymph nodes, where they enter the paracortical areas, the home of naive T lymphocytes. Probably while en route to the lymph node, the Langerhans' cells process the sensitiser so it is physically associated with the HLA-DR molecules on the cell surface. In the node, the Langerhans' cells "present" the sensitiser to T lymphocytes of the immune system. If T cells with the appropriate specific receptor recognise the complex of sensitiser and HLA-DR, they proliferate to establish "immunological memory." The memory T cells that mediate allergic contact eczema are of the Th1 subtype, characterised by the production of interleukin 2 and interferon gamma. The induction of sensitisation and establishment of immunological memory takes 8-14 days. Should re-exposure to the sensitiser occur, Langerhans' cells carry it down into the dermis, where they present it to memory T cells travelling through the tissues. These are activated to release cytokines (including interferon gamma) that attract other cells and activate vascular responses, resulting in the characteristic inflammation of contact eczema.

View larger version (103K): [in this window] [in a new window]   Irritant contact eczema (dermatitis) of the hand

Differential diagnosis
Allergic contact eczema must be distinguished from irritant contact eczema. Clinically the two may be indistinguishable, but irritant eczema usually occurs on the hands. It is the result of repeated "insult" to the skin with caustic, irritant, or detergent substances. Photoallergic eczema occurs on light exposed areasface, nape of neck, and backs of hands. It is usually a response to photosensitisation by ingested drugs such as thiazide diuretics or quinine.

View larger version (82K): [in this window] [in a new window]   Patch testing for diagnosing causal sensitiser in allergic contact eczema

Management
The causal agent should be identified by epicutaneous patch tests. Contact allergy can be induced by a huge range of substances encountered daily. Sometimes the history of flare ups after contact with something is sufficient to permit reasonably confident identification. Often a short list of possible culprits can be arrived at. Definitive proof of causal significance, however, requires patch testing. This is normally performed in dermatology clinics with the requisite expertise and range of test materials.

	Atopic eczema

Definition
The atopic state is a genetically determined capacity to make IgE class antibodies to antigens that enter the body via mucosal surfaces. This is associated with allergies of the immediate type and the clinical syndromes of rhinitis asthma or atopic eczema, alone or in combination.

Prevalence
For unclear reasons the prevalence of atopic diseases, including eczema, has risen steadily over the past 30 years. There are many estimates of the prevalence of atopic eczema in children in different countries. For children aged up to 12 years these range from 12-26%.

View larger version (88K): [in this window] [in a new window]   Typical atopic eczema in child

Aetiology
In atopic individuals, responses to common allergens result in the generation of helper T lymphocytes of the so called Th2-type in preference to those of Th1-type.

Clinical presentation
Atopic eczema most commonly begins in infancy. The rash of erythematous areas comprises tiny papules, sometimes with an urticaria-like component. They may join to form confluent red sheets. In infants atopic eczema commonly affects the whole body including the head and face. On the limbs predominantly extensor surfaces are affected.

View larger version (78K): [in this window] [in a new window]   Discoid pattern of atopic eczema

Complications
Immune resistance to several microbial pathogens is reduced in individuals with atopic eczema. Thus both viral warts and molluscum contagiosum can be numerous and slow to clear. Eczema herpeticum is infection with herpes simplex viruses, which may be extensive and aggressive.

View larger version (80K): [in this window] [in a new window]   Eczema herpeticum (ulcers are of similar shape and size)

Management

Drug treatment
The basis of direct treatment is to suppress the symptoms and control or prevent complications.

Atopic eczema is readily irritated by soaps, so their avoidance and use of emollients as soap substitutes is important.

Anti-inflammatory topical steroids are the mainstay of treatment. In children, when the eczema is very active, stronger steroids such as betamethasone valerate (1/4 strength) may be required. Normally, clobetasone or mometasone may be adequate for treating areas other than the face; 1% hydrocortisone is the main steroid for the face. In adults undiluted category 3 steroids may be required for flare ups. Dilutions and weaker steroids are used for regular maintenance.

Acute flares are often induced by staphylococcal superinfection. Systemic antibiotics (flucloxacillin or erythromycin) should be used. If chronic or repeated infective episodes occur, use of a topical steroid and antibiotic, or antiseptic mixtures, can help.

Although antihistamines are often used to relieve itch, histamine is not the main, responsible mediator. Hence antihistamines are not very effective, and usually the older sedative typessuch as trimeprazine, hydroxyzine, and chlorpheniramineseem more effective than the modern non-sedative varieties.

Bandages and dressings
In infants and children the "wet bandage" technique can provide great symptomatic relief. A double layer of medium grade tubular cotton bandage (Tubifast, Seton) is applied over a layer of emollient or sometimes over a weak topical steroid. The inner layer of bandage is moistened with warm water. The dressing can be applied to limbs and even the trunk. For very lichenified or excoriated eczema, various bandages impregnated with antiseptics (Ichthopaste, Smith and Nephew, or Quinaband, Seton) or zinc oxide (Viscopaste, Smith and Nephew) can be used to occlude the area; a weak steroid and antiseptic mixture is usually applied underneath.

View larger version (28K): [in this window] [in a new window]   Effect of avoiding house dust mite allergens on severity of atopic aczema. Individual scores before and after 6 months' avoidance are connected by fine lines. Solid lines represent median scores for each group

Second line treatment
Systemic corticosteroids should be used very seldom. Atopic eczema virtually always flares rapidly on dose reduction. Ultraviolet light (UVB) and photochemotherapy with a psoralen and long wavelength ultraviolet irradiation (UVA; PUVA) may be used in older children and adults.

Third line treatment
When second line treatment fails or is not suitable, various further treatment options are available (see box).

Allergen avoidance
The role of allergen avoidance should be considered for all patients with atopic eczema. Avoidance or elimination of house dust mite allergens can be beneficial for many people with confirmed mite sensitivity who have severe atopic eczema. The main study to show this looked at children aged over 6 years and adults. The most important measures are encasing the mattress in a dust proof bag, and washing the duvets and pillows every three months; washes should be hotter than 55°C to kill mites and denature antigens. Removal of fitted carpets in the bedroom should be recommended. Reducing upholstered furnishings and regular use of a modern cylinder or upright vacuum cleaner fitted with an adequate filter seem sensible precuations.

Foods are often suspected as being provoking factors in babies, but reliable identification of relevant foods is difficult and often impossible. Hence regimens avoiding dairy or other suspected foods are often disappointing, and if no clear benefit is obtained they should not be maintained for longer than four weeks. In small children such diets are difficult to implement, and the help of a dietician is necessary.

	Acknowledgments

The photograph showing dermatitis of the hand is reproduced with the permission of Gower Medical Publishing. The data in the graph are adapted from Tan et al (Lancet 1996;347:15-8).

P S Friedmann is professor of dermatology at Southampton General Hospital.

The ABC of allergies is edited by Stephen Durham, honorary consultant physician in respiratory medicine at the Royal Brompton Hospital, London. It will be published as a book later in the year.    BMJ 1998;316:1226-9